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Original Author(s): Christian Tang
Last updated: 20th December 2020
Revisions: 7

Original Author(s): Christian Tang
Last updated: 20th December 2020
Revisions: 7

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The B lymphocyte (B cell) is one of the most important cells of the body. They form part of the adaptive immune response by producing antibodies and presenting antigens to T cells. Once activated, they can mature into plasma cells or memory B cells.

This article covers B cell development and subtypes.

B Cell Development

B and T lymphocytes arise from common lymphoid progenitor cells within the bone marrow. The progenitor cells that are committed to the B cell lineage (as opposed to the other lymphocyte types, e.g. T cells and NK cells) are selected at random. T cell progenitors migrate to the thymus for maturation. However, B cell progenitors remain in the bone marrow.

Two selection processes happen during B cell development; both of which depend on the B cell receptor. Positive selection ensures that only B cells with functional receptors are allowed to develop. It happens when the B cell receptor successfully binds its ligand, consequently allowing the B cell to receive survival signals. Negative selection happens when B cells respond to self -antigens in the bone marrow and, as a result, undergo receptor editing, anergy or apoptosis. This promotes central tolerance and minimises the risk of autoimmune reactions when the B cells eventually mature and move to the peripheral circulation.

Once differentiated in the bone marrow, B cells migrate to lymphoid follicles in the spleen. They also migrate to areas where lymphoid activation and defence is likely to be triggered, e.g. in the mucosal linings as associated lymphoid tissue. An example of this, are The Peyer’s patches of the colon, which are mucosa-associated Lymphoid tissue (MALT). Other ‘MALTs’ also exist and are named according to their location or organisation e.g. Bronchial (BALT), Nasal (NALT), Organised-mucosa (O-MALT).

 

Types of B Cell

Plasma Cell

Once activated, B cells can differentiate into plasma cells. Plasma cells are large lymphocytes with abundant endoplasmic reticulum, which allows them to produce large quantities of antibodies against specific antigens.

They respond to signals from T cells during infection and continue to produce antibodies until the infection is controlled. Plasma cells are often found with chronic inflammation.

B cells, plasma cells, histology.

Fig 1 – Blood film showing a multinucleated plasma cell

Memory B Cell

Some B cells will differentiate into memory B cells when activated. These are long-lived cells which remain within the body and allow a more rapid response to future infections.

If the host is re-exposed to the same antigen, these cells rapidly proliferate with assistance from T cells. This produces more B cells capable of secreting specific antibodies to the pathogen. This often means that the pathogen can be dealt with before the infection takes hold and becomes symptomatic.

T-independent B Cells

Most B cells require T cells to produce antibodies. However, a small number can function without T cell help. They are found within specialised sites such as the spleen and peritoneum.

They are particularly important for dealing with encapsulated bacteria. Encapsulated bacteria have a polysaccharide outer layer as opposed to a protein-based one, which allows them to evade T cells. T-independent B cells can recognise these layers and produce antibodies without T cell help.

Clinical Relevance – X-linked Agammaglobulinemia (XLA)

XLA, also known as Burton’s disease, is a rare genetic disorder that affects the body’s ability to fight infection. Patients are unable to produce mature B cells, as such, they tend to have an absence of serum immunoglobulins post 6 months (after maternal IgG have been broken down).

Like many primary immune deficiencies, patients typically present with infections that are severe, persistent, uncommon and recurrent.  Haemophilus influenzae, Streptococcus pneumoniae, and staphylococci are common causative pathogens.

It is generally diagnosed by genetic testing.

Treatment is with immunoglobulin replacement therapy and patients may also require prophylactic antibiotics. Patients with XLA should not receive live vaccines.